KELOMPOK 5A

Alfannya Alvin 1810311006

Bella Alvina Lim 1810312047
Fikri Fadhil 1810313020
Fino Nauvalino 1810313024
Fitria Rahmi Nukti 1810312035
Muhammad Luthfi 1810312013
Salma Aulia Zahirah 1810312048
Sherly Febrina 1810311028
Suci Berlian Hemilton 1810311033
Suci Rahmayeni 1810313041
SKENARIO
STEP 1
STEP 2
STEP 3
STEP 4
STEP 5
HYPERTENSION
LO 1 Classification of Hypertension
• 1. Essential (primary) hypertension: systolic and dystolic
blood pressure conditions are more than normal, for which
the cause is not known with certainty (idiopathic).

• 2. Secondary hypertension: systolic and dystolic blood

pressure conditions are more than normal, which is
caused by disorders of the kidneys, endocrine system, or
vascular.
LO 2
Epidemiology, etiology, and risk factor

Epidemiology

• ccording to the NHLBI (National Heart, Lung and Blood

Institute), 1 in 3 patients suffer from hypertension
• The prevalence of hypertension in Indonesia is 26.5%
(Riskesdas 2013)
Etiology

• Primary / essential hypertension (incidence 80-95%)

Hypertension of unknown cause. Many factors influence it,
such as genetics, environment, hyperactivity of the
sympathetic nervous system, angiotensin renin system,
defects in Na excretion, intracellular Na and Ca memory, and
factors that can increase risks such as diabetes, obesity,
smoking, alcohol, and polycythaemia.
• Secondary hypertension
As a result of an underlying disease or disorder such as renal
artery stenosis, renal parenchymal disease,
pheochromocytoma, and primary hyperaldosteronism
Risk Factors

1) Age
2) Race / ethnicity
3) Gender
4) Unhealthy Lifestyle Habits. An unhealthy lifestyle
can increase hypertension, including drinking alcoholic
beverages, lack of exercise, and smoking.
LO 3 Pathogenesis and Pathophysiology
Pathogenesis

Hypertension is a multi factorial disease. Various mechanisms

that play a role in increasing blood pressure, including:
1) Neural : Stress, sympathetic activity
2) Renal : High sodium intake with fluid retention
3) Vascular : Endothelial dysfunction, free radicals, and blood
vessel remodeling
4) Hormonal : The renin-angiotensin-aldosterone system
Pathophysiology

The pathophysiology of hypertension is through the formation of

angiotensin II from angiotensin I by angiotensin I converting
enzyme (ACE). ACE plays an important physiological role in
regulating blood pressure. Blood contains angiotensinogen which
is produced in the liver. Furthermore, the renin hormone will be
converted into angiotensin I. By ACE in the lungs, angiotensin I
is converted to angiotensin II.
Renin is synthesized and stored in an inactive form called
prorenin in juxtaglomerular cells (JG cells) in the kidneys. JG
cells are modifications of smooth muscle cells located in the
walls of the afferent arterioles right in the proximal glomeruli.
When arterial pressure decreases, the intrinsic reaction in the
kidney itself causes many protein molecules in JG cells to break
down and release renin.
 Angiotensin II is a very powerful vasoconstrictor and has other
effects that also affect circulation. As long as angiotensin II is in
the blood, angiotensin II has two main effects that can increase
arterial pressure.
The first effect, namely vasoconstriction, arises quickly.
Vasoconstriction occurs mainly in arterioles and is slightly weak
in veins. The second effect, where angiotensin II increases arterial
pressure is by working on the kidneys to reduce the excretion of
salt and water.
Aldosterone, which is secreted by glomerulose zone cells in the
adrenal cortex, is an important regulator for the reabsorption of
sodium (Na +) and potassium (K +) secretion by the renal
tubules. The main place of action of aldosterone is in the
principal cells in the cortical tubule reabsorption. Aldosterone
also increases sodium permeability on the luminal side of the
membrane.
 • Headache
LO 4 • Nausea and vomiting
Clinical • Blurred vision
Presentation • Nokturia
• Edema
• dizzy, flushing, nosebleed ,
neck sore
LO 5
1. DIAGNOSIS HIPERTENSI
• Joint National Committee VII :
- At least,two measurements of blood pressure at different
times
- The first measurements -> was confirmed at least two
more visits in one to several weeks

Uphold if from repeated measurements obtained

an average value of diastolic blood pressure
≥ 90 mmHg and or systolic blood pressure ≥ 140
mmHg.
 History Physical
Talking Examination

Lab Supporting
Examination investigation
KLASIFIKASI HIPERTENSI JNC VII
Clinical Manifestation

“Silent Killer”
On physical examination, not found any
abnormalities other than high blood pressure,
but can also be found changes in the retina,
such as bleeding, exudate (a collection of
fluids), narrowing of blood vessels, and in
severe cases will experience pupillary edema
Headache when awake, sometimes accompanied by
nausea and vomiting, due to increased intracranial
blood pressure

Blurred vision due to damage to the retina

Nocturia due to increased renal blood flow and

glomerular filtration

Edema due to increased capillary pressure

SUPPORTING EXAMINATION

1) Urea and creatinine examination

2) Potassium check in serum
3) Calcium examination
4) GDS examination
5) Urinalysis examination
6) EKG examination
7) Thorax Photo
2) Deep Vein Thrombosis
LO 6
LO 7 Complication and Prognosis
VASCULAR DISEASE
LO 1 Classification of Vascular disease
1. Chronic venous insufficiency: the condition of persistent
venous hypertension especially in the lower extremities due to
obstruction or incompetence of venous valves, so that venous
blood flow is reversed (venous reflux) in the congested limbs.
2. Peripheral arterial occlusion disease: a condition in which
blood flow to the limbs becomes blocked due to narrowing of
blood vessels originating from the heart (arteries).
3. Deep vein thrombosis: Conditions when blood clots occur in
one or more deep vein blood vessels.
4. Abdominal aortic aneurysm: a prominent or swollen part of
the aorta that passes through the stomach. This aorta is the
largest aorta that originates from the heart to the lower chest to
the abdomen, which starts when the aortic wall weakens.
LO 2
Epidemiology, etiology, and risk factor
Chronic venous insufficiency
• Abnormalities including telangiectasia, reticular, varicose
veins, ankle edema, and skin changes and varicosal
ulcers. The term varicose veins - abnormalities of the vein
system that extend, widen, twist, and valve disorders.
• Chronic venous insufficiency is found in 25-50% of adult
women and 15-30% of adult men.
Etiology

Congenital: no formation of superficial vein valves and

communicants from birth
Obtained: thrombus formation resulting in impaired
venous blood flow, chronic lesions that do not heal (eg
ulcers in the lower extremities), valvular insufficiency in
deep veins, and deep vein thrombosis
Risk Factors

• Age
• Female gender
• Obesity
• Sit or stand still for long periods of time
Peripheral Arterial Occlusion Disease
Peripheral Arterial Disease (PAD) or can also be called
Peripheral Arterial Occlusive Disease (PAOD) is a blockage
in the peripheral arteries due to the process of
atherosclerosis or inflammatory processes that cause the
arterial lumen to narrow (stenosis), or thrombus formation.
Epidemiology :

• There are 1 in 20 people over the age of 50, or 8 million in

the United States
• Prevalence: >> 55 years is around 10-25%
• 70 - 80% asymptomatic
• Only diagnosed 50% of the population
• The cause of peripheral arterial occlusion is the presence
of stenosis (narrowing) of the arteries which can be
caused by atherosclerosis reaction or inflammatory
reaction of blood vessels which causes the lumen to
narrow.
• Risk factors for peripheral arterial occlusion are smoking,
a diet high in fat or cholesterol, stress, a history of heart
disease, heart attack, stroke, obesity, diabetes, and
abnormalities in protein synthesis such as protein C and
protein S.
Deep Vein Thrombosis
• Deep Vein Thrombosis (DVT) is a blood clot that occurs in
the veins (veins) in the inside. The blocked vein flow is the
cause that often begins TVD.
• The incidence of DVT is 1 in 1000 people where 1-5% die
due to complications caused.
Etiology

• Injury to veins
• Increased risk of thrombus
• Slower blood flow to veins
Risk Factors

1. Sit for too long 8. Heart failure

2. Has a history of blood 9. Pacemaker and catheter
clotting disorders in the vein
3. Bed Rest 10. Has a history of TVD
4. Injury or surgery or pulmonary embolism
5. Pregnancy 11. Having excess weight
or obesity
6. Cancer
12. Smoking
7.Inflamatory bowel
13. Old age (over 60 years)
sydnrome
14. Has a high height
Abdominal Aortic Aneurysm
• Aneurysms are segmental (focal) arterial dilatation, with
an increase of more than 50% of the normal diameter.
This condition involves thinning of the three layers of the
blood vessel wall.
• There are several causes of aneurysmal dilatation. A
small number of AAA cases are a direct result of certain
causes such as trauma, acute infections (Brucellosis,
Salmonellosis), chronic infections (turbekulosis),
inflammatory diseases (Behcet's disease, Takayasu) and
connective tissue diseases such as Marfan Syndrome,
and Danlos type IV. While most of AAA is non-specific,
with several risk factors associated with it
• Important risk factors for the occurrence of AAA are old
age, male sex, smoking and family history of AAA.
• The incidence of AAA in men is 5 times more than in
women. Old age has long been associated with AAA. The
prevalence of AAA events between the 45 to 54 years and
75 to 84 years age groups increased from 2.6% to 19.8%
in men.
• the incidence of AAA varies 4 to 7 times more than in the
nonsmoking group. Nearly 30% of AAA cases are related
to family history.
Aneurysm formation is a complex factor and involves
several processes, namely;

matrix degradation by proteolytic enzymes

transmural inflammation
immunological response
genetic influence
increased bimechanical wall stress and atherosclerotics
LO 3 Pathogenesis and Pathophysiology
Deep Vein Thrombosis
Patophysiology

Thrombus that forms in the iliac vein and the proximal femoral
vein can escape from its place and follow the bloodstream
(embolism) to the heart and lungs. The presence of embolism can
then clog arteries in the lungs, causing pulmonary embolism.
Small emboli will clog the lung capillaries causing lung tissue
infarction. However, if the embolism is large enough, partial
blockages can occur or even the entire blood flow from the right
ventricle and cause death
LO 4 Clinical Presentation
DEEP VONOUS THROMBOSIS (DVT)
• Thigh discomfort when standing or walking
• Unilateral leng swelling
• Edema
• Erythema
• Warmth
• Can be superficial blood vessels
• The homan sign +
ABDOMINAL AORTIC ANEURYSMS (AAA)

• Most aneurysms are asymtomatic

• Abdominal : pulsatile mass
• Abdominal or back pain
• Dilatation of the vessel
CHRONIC VENOUS INSUFFCIENCY (CVI)
• Pain or achiness in the legs when standing for prolonged
periods
• Varicose veins
• Edema
• Skin in inflammation and hyperpigmentations
• Ulcerations
PHERIPHERAL ARTERY DISEASES (PAD)
• Thigh calf discomfort when walking and relieved by rest
• Claudication
• The cronically : ulceration, infection, skin necrosis
LO 5
1 ) DIAGNOSIS PERIFER
ARTERIAL DISEASE
- vascular physical examination, including auscultation of the femoral artery,
palpation of peripheral pulses and skin inspection

- laboratory test
- Measurement of limb pressure using Ultrasound Doppler to assess distal blood
flow is a key examination in patients with peripheral heart disease and can be
done at rest or while doing exercise (treadmill).
The Ankle Brachial Index (ABI), is a measure to determine the ratio of systolic pressure in the
-
ankle (greater pressure on the posterior tibia and dorsal pedis artery) to systolic pressure in
the brachial artery, usually used to diagnose and determine the degree of peripheral vascular
disease (ABI score score) <0.90 indicated by peripheral artery disease).
- Computed Tomography Arteriography (CTA)
- Magnetic resonance arteriography (MRA)
2) Deep Vein Thrombosis
1. Venography
2. D-dimer Test
3. USG Doppler
 3) Chronic Venous Insuficiency
1) Duplex Doppler ultrasonography
This type of ultrasound procedure is performed for the assessment of
blood vessels, blood flow and structure of the veins.
2. Venography
Done using x-ray and intravenous (IV) contrast dye to visualize blood vessels.
Contrasting causes blood vessels to appear bleak on x-ray imaging, which makes it
easy to visualize the blood vessels being evaluated

3) Plestimografi Vena
The pletismographic technique detects changes in venous blood volume in the limbs
4) Aneurisma Aorta Abdominal
To determine the diagnosis of an abdominal aortic aneurysm, the
doctor can evaluate the medical history of the patient and family
members and do a physical examination directly. If an abdominal aortic
aneurysm is suspected, several investigations can be carried out, such
1. Ultrasound (USG) of the abdomen. This examination is most often done to
as:
diagnose an abdominal aortic aneurysm, using sound waves to produce
imaging of the abdomen.
2. Computerized tomography (CT). This examination can also produce a clear
image of the aorta, and can detect the size and shape of the aneurysm. This
examination uses X-ray waves to produce imaging of body organs. The
doctor can also inject a dye into the blood vessels to make arteries more
visible on CT images, which are called CT angiography.
3. Magnetic resonance imaging (MRI). This examination can also be aimed at
diagnosing an aneurysm and determining its size and location. MRI
examination uses a magnetic field and radio waves to produce imaging of
the body's organs.
The doctor can also inject dye into the blood vessels to make the blood vessels
more visible on the results of imaging, which is called MR angiography.
LO 6 PROCEDURES FOR HYPERTENSION AND VASCULAR DISORDERS
HYPERTENSION
All patients with hypertension must have lifestyle
modifications. Criteria for starting anti-hypertension:
• Patients with first-degree hypertension with at least one of
the following ailments
• Injury to the target organ
• History of MY disease
• Kidney illness
• DM
• RK in 10 years ≥ 20%
• All patients with grade 2 hypertension
• After giving antihypertensive drugs, monitor and evaluate
the patient.
Lifestyle modification:
• Weight loss: Asia Pacific target 18.5 - 22.9 kg / m2 →
systolic reduction 5-20 mm / Hg / 10 kg
• Diet (Dietary Aproaches to Stop Hypertension - DASH) →
decrease in systolic 8-14 mmHg (includes consumption of
fruits, vegetables, and low-saturated / total fat dairy
products)
• Decreased salt intake, recommended NaCl consumption
<6 g / day → decrease in TDS 2-8 mmHg
• Physical activity for at least 30 minutes / day, done at
least 3 days a week decrease → 4 - 9 mmHg
• Restrictions on alcohol consumption
NICE
• Age <55 years → L1: ACE / ARB inhibitors → L2: ACE /
ARB + CCB inhibitors → L3: ACE / ARB + CCB +
thiazides inhibitors → L4: ACE / ARB inhibitors + CCB +
thiazides + other diuretics / αBlocker / βBlocker →
Monitoring & evaluation
• Age> 55 years → L1: CCB → L2: ACE / ARB + CCB
inhibitors → L3: ACE / ARB + CCB + thiazid inhibitors →
L4: ACE / ARB + CCB inhibitors + thiazides + other
diuretics / αBlocker / βBlocker → Monitoring & evaluation
JNC VIII
CHRONIC VENA INSUFFICIENCY
Non Medical
• Patients are advised to actively move and not maintain a
position for too long. If forced to sit or stand for long
periods of time, it is important to elevate the leg up and
down
• Foot elevation (about 15 cm high)
• BB controlled
• Regular exercise, it is important to remember to avoid
sports that are too heavy and intensive, especially those
that can increase venous pressure (such as badminton)
Medical
• Compression
• Physiotherapy
• Invasive procedures: sclereotherapy, phlebectomy, or
abena safna vein ablation with surgery
• Hydrosmin supplement 3 x 200 mg / oral
ARCHIVE PERIFER OKLUSION DISEASE
Non-Medical Therapy
• Modification of risk factors
• Light intensity regular exercise is recommended for
claudication patients, such as treadmill training and
walking with a duration of every 50 minutes with each
exercise, interspersed to rest every 5-10 minutes
Medical therapy
• Includes symptomatic therapy and FR control: aspirin or
acetyl salicylic acid dose 75 - 325 mg / day orally;
Clopidogrel 75 mg / day orally
• Revascularization Procedure
DVT
Prevention
• Elastic socks
• Anticoagulants: Low-dose Heparin is given 0.2 ml
subcutaneously 2x a day for 5-7 days
Medical
• Anticoagulant therapy
• Heparin: Indications, definitive: acute DVT, pulmonary
edema. Doses of 80 IU / kg body weight (around 10-14 days
and warfarin starts 4 - 6 days before heparin is stopped)
• Thrombolytic Therapy
Therapy compression and evaluation
Endovascular therapy
AORTA ABDOMINALIS ANEURISM
• The goal of treatment for aortic aneurysms is to prevent
aneurysms from getting bigger and to prevent aneurysm ruptures.
If the size of the aneurysm is still small and the patient does not
feel any symptoms, the patient performs routine controls to
monitor the development of the aneurysm.
• In addition to routine control, can provide drugs to prevent or
minimize the risk of aortic rupture. Some medicines that will be
given are:
• Statin drugs, to reduce choleceterol and reduce the risk of aortic
blockage due to atherosclerosis
• Beta blockers or beta blockers, to lower blood pressure by
slowing the heart rate
• AngiAangiotensin 2 receptor blockers (ARBs), to lower blood
pressure if beta blocking drugs do not work effectively
• If the size of the aneurysm has reached more than 5.5 cm, surgery is
performed. Surgery will also be recommended for patients who have a
family history of aortic dissection or Marfan syndrome, even though
the size of the aneurysm is still small. The operation needs to be done
as an emergency treatment if the aneurysm has broken or torn.
• Some types of operations to treat aortic aneurysms are:
• Open surgery
• This operation is done by removing the aortic part that is bulging
and replacing it with new blood vessels
• End Endovascular surgery
• This procedure is less invasive. Endovascular surgery is done by
placing a stent or ring on the aneurysm using a catheter. Stents
strengthen the walls of the aortic vessels that are weak and
prevent the rupture of these vessels
After undergoing surgery, live a healthy lifestyle. This
healthy lifestyle is also beneficial for reducing the risk of
ruptured aneurysms.
• Quit smoking
• Avoid heavy thoughts that cause stress
• Avoid heavy physical activity, such as weight lifting
• Reducing fat intake so that cholesterol levels fall
LO 7 Complication and Prognosis
VENOUS CHRONIC INSUFFICIENCY
Prognosis

The prognosis for ulcer healing and inflammation is quite

good without concomitant diseases. The majority of patients
without complications respond well to outpatient treatment
as it supports in the "treatment" section. Permanent
changes include hemosiderosis and fibrosis that occur
before starting therapy. Loss of active valve function is
irreversible. There is no sustained cutaneous support in the
long term in the form of an inelastic cover or elastic
stocking, it can renew injury injuries to the skin and soft
tissue.
Peripheral Artery Disease
Complications

schemic ulceration, gangrene, neuropathic ischemia and

Leriche syndromePAOD can cause chronic complications
such as ischemic ulceration, progressive gangrene which
then requires action. Other complications can arise as a
resultoperative therapy of arterial reconstruction, anesthesia,
and major surgery, namely infection by MRSA in the graft and
occlusion due to graft failure. Complications must be handled
early, right, and good because it can be bad for patients if
treatment is late. Therefore a good relationship between the
surgeon and other experts and careful perioperative care is
needed to detect any unexpected complications.
Prognosis

Difficulty in determining diagnosis criteria due to unclear

clinical manifestations so that P AOD still has a fairly high
morbidity and mortality rate.Diabetes is also strongly
associated with the development of symptoms of
intermittent claudication and further worsens the prognosis
of this disease.
Deep Vein Thrombosis
Complications

• Complications of Lung Embolism

• Thrombus which is released into embolus will follow the
blood flow to the heart and will be flowed to the branches
of the arteries in the lungs so that it will inhibit blood flow.
Patients with EP often complain of sudden tightness
accompanied by hemoptysis or chest pain or chest pain
and sudden collapse with shock and even sudden death.
About 10% of untreated TVD sufferers develop pulmonary
embolism which causes severe symptoms or death.
Prognosis

DVT mortality is mainly related to the incidence of pulmonary

embolism, in which there are as many as 300,000 deaths per year
in the United States. According to statistics from the Centers for
Disease Control and Prevention (CDC), around 10-30% of patients
die within the first 1 month of being diagnosed with venous
thromboembolism, and sudden death is the first symptom in a
quarter of cases of pulmonary embolism.
The main long-term morbidity of DVT is post-thrombotic syndrome
(PTS). A 2004 publication in the United States covering 21,680
subjects aged ≥45 years who were monitored for 7.6 years
recorded a 7.7% recurrence within 2 years after the first episode of
venous thromboembolism. According to CDC data, half of DVT
sufferers will experience PTS complications such as swelling, pain,
or skin discoloration. Additionally, one third of DVT sufferers are
recorded to have recurrences within 10 years.
Aortic Aneurysm
The main complication that can be suffered by people with
aortic aneurysm is a torn or broken aortic wall. Symptoms
of aortic wall rupture include:
• Severe pain that appears suddenly in the abdomen,
chest, or back
• Difficulty breathing
• Low blood pressure (hypotension), even to shock
• Pain radiates to the back or legs
• Excessive sweating
• Shortness of breath
• Hard to swallow
• Nausea and vomiting
• Heart beats fast
• Dizziness and loss of consciousnessIn addition, aortic
aneurysm can also cause complications in the form of:
• Aortic regurgitation, a condition when the aortic valve
does not close completely so that blood flows back into the
heart
• The appearance of blood clots that can block blood flow
• Renal failure due to lack of blood flow into the kidneys
• Inflammation and damage to intestinal tissue due to lack
of blood flow to the intestine
Prognosis

strongly influenced by the presence or absence of

aneurysm rupture. Rupture is a medical emergency
condition associated with a high risk of death (> 50%), both
for abdominal aortic aneurysms and thoracic. However, the
survival of aortic aneurysm patients tends to be high as long
as the patient gets adequate treatment, it can even be close
to the population without aortic aneurysm.